536 RADIATION BIOLOGY 



plying power by mutations of the recessive autosomal type studied in this 



work. 



However, essentially the same disturbance is at work here as in the 

 maize pollen, namely, inequality in absorption (and conceivably, in this 

 case, in sensitivity, which would have a similar effect). The sperma- 

 tozoa in different portions of the long spiral testes, and even those in 

 different individuals, are shielded to very different extents by the over- 

 lying layers, and the polar cells, although much more directly exposed, 

 are, nevertheless, unequally illuminated also, especially since they lie in 

 approximately two layers. In order to explain the findings at the higher 

 doses on this basis it is necessary, in addition, to take into consideration 

 the fact (supported by considerable evidence) that the more strongly 

 illuminated cells (and perhaps the more mutagenically sensitive ones, if 

 there are generalized differences in sensitivity also) undergo more physio- 

 logical incapacitation. Thus those with more mutations would tend (but 

 not in this case because of their mutations) to be selectively eliminated to 

 an increasing extent at higher doses. This still would not explain the 

 actual drop in rate at higher doses found for the spermatozoa, unless the 

 differences in illumination and/or sensitivity were more or less discon- 

 tinuous, giving a distribution of effects which was bi- or poly modal, but 

 this situation is very hkely to exist. 



It does, however, seem a stretch of plausibility to suppose that the 

 differences in illumination and sensitivity of even the pole cells are great 

 enough and varied enough in amount to allow an approximate maximum 

 frequency to be maintained over a range of doses whose extremes differ 

 from each other by about five times, as was found in some of the work. 

 It is therefore probable that still another factor is operating to prevent 

 the mutation frequency from rising at high doses or to cause its actual 

 decline, namely, a factor which tends to counteract the production or 

 completion of the mutational events. This possibility would to some 

 extent correspond with Hollaender and Emmons's (1941) suggestion that 

 perhaps the soaking of the fungus spores allowed mutations to come "to 

 completion" which otherwise would not have done so. For the latter 

 postulate would, when followed through, imply that, without the soaking, 

 a considerable proportion (increasing with dose) of potentially mutant 

 cells finally become normals, whereas, with the soaking, fewer of them 

 become normals. According to this kind of interpretation, something 

 connected with the ultraviolet treatment must be preventing the muta- 

 tions from becoming effectuated, and this effectuation can occur a long 

 time after irradiation. 



It is noted in the next section that a process or processes of repair of 

 ultraviolet effects, promoted among other things by ultraviolet itself, does 

 in fact exist. It was postulated by Muller (Muller, 1949 ; Altenburg et al, 

 1949; see also Muller, 1952a, c), before this repair had been shown to 



